&nbsp;robusta-infected roots, while levels of SA and ROS were significantly higher in I.&nbsp;mors-panacis-infected roots. Catalase activity was significantly higher in I.&nbsp;robusta-infected roots followed in order by mock roots and those infected by I.&nbsp;mors-panacis. Moreover, I.&nbsp;mors-panacis was resistant to ROS compared with I.&nbsp;robusta. Conclusion Infection by the weakly aggressive I.&nbsp;robusta led to the upregulation of ginsenoside production and biosynthesis, probably because only a low level of ROS was induced. In contrast, the more aggressive I.&nbsp;mors-panacis suppressed ginsenoside biosynthesis, probably because of higher ROS levels and subsequent induction of programmed cell death pathways. Furthermore, I.&nbsp;mors-panacis may have increased its virulence by resisting the cytotoxicity of ROS. © 2019 The Korean Society of Ginseng, Published by Elsevier Korea LLC.Background The patatin-related phospholipase AIII family (pPLAIIIs) genes alter cell elongation and cell wall composition in Arabidopsis and rice plant, suggesting diverse commercial purposes of the economically important medicinal ginseng plant. Herein, we show the functional characterization of a ginseng pPLAIII gene for the first time and discuss its potential applications. Methods pPLAIIIs were identified from ginseng expressed sequence tag clones and further confirmed by search against ginseng database and polymerase chain reaction. A clone showing the highest homology with pPLAIIIβ was shown to be overexpressed in Arabidopsis using Agrobacterium. Quantitative polymerase chain reaction was performed to analyze ginseng pPLAIIIβ expression. Phenotypes were observed using a low-vacuum scanning electron microscope. Lignin was stained using phloroglucinol and quantified using acetyl bromide. Results The PgpPLAIIIβ transcripts were observed in all organs of 2-year-old ginseng. Overexpression of ginseng pPLAIIIβ (PgpPLAIIIβ-OE) in Arabidopsis resulted in small and stunted plants. It shortened the trichomes and decreased trichome number, indicating defects in cell polarity. Furthermore, OE lines exhibited enlarged seeds with less number per silique. The YUCCA9 gene was downregulated in the OE lines, which is reported to be associated with lignification. https://www.selleckchem.com/products/chloroquine-phosphate.html Accordingly, lignin was stained less in the OE lines, and the expression of two transcription factors related to lignin biosynthesis was also decreased significantly. Conclusion Overexpression of pPLAIIIβ retarded cell elongation in all the tested organs except seeds, which were longer and thicker than those of the controls. Shorter root length is related to auxin-responsive genes, and its stunted phenotype showed decreased lignin content. © 2019 The Korean Society of Ginseng, Published by Elsevier Korea LLC.Background Ginseng (Panax ginseng Meyer) is an essential source of pharmaceuticals and functional foods. Ginseng productivity has been compromised by high light (HL) stress, which is one of the major abiotic stresses during the ginseng cultivation period. The genetic improvement for HL tolerance in ginseng could be facilitated by analyzing its genetic and molecular characteristics associated with HL stress. Methods Genome-wide analysis of gene expression was performed under HL and recovery conditions in 1-year-old Korean ginseng (P.&nbsp;ginseng cv. Chunpoong) using the Illumina HiSeq platform. After de novo assembly of transcripts, we performed expression profiling and identified differentially expressed genes (DEGs). Furthermore, putative functions of identified DEGs were explored using Gene Ontology terms and Kyoto Encyclopedia of Genes and Genome&nbsp;pathway enrichment analysis. Results A total of 438 highly expressed DEGs in response to HL stress were identified and selected from 29,184 representative transcripts. Among the DEGs, 326 and 114 transcripts were upregulated and downregulated, respectively. Based on the functional analysis, most upregulated and a significant number of downregulated transcripts were related to stress responses and cellular metabolic processes, respectively. Conclusion Transcriptome profiling could be a strategy to comprehensively elucidate the genetic and molecular mechanisms of HL tolerance and susceptibility. This study would provide a foundation for developing breeding and metabolic engineering strategies to improve the environmental stress tolerance of ginseng. © 2019 The Korean Society of Ginseng, Published by Elsevier Korea LLC.Extracts of ginseng species show antihyperglycemic activity. We evaluated the inhibitory effects of diabetic complications for Korean Red Ginseng (KRG), which is enriched in ginsenosides using Otsuka Long-Evans Tokushima Fatty (OLETF) rats. The animals were divided into one of four groups (n&nbsp;=&nbsp;6?9) Long-Evans-Tokushima-Otsuka&nbsp;rats (control rats), OLETF&nbsp;rats, rats given 200 mg/kg KRG, and rats given 400 mg/kg KRG. We examined the protective potential of KRG against type 2 diabetic illnesses. The results exhibited that KRG showed significant antihyperglycemic and antioxidative effects in KRG-treated OLETF rats. And, our results proposed the amelioration of cardiac function through normalized ejection fraction, fractional shortening, and vascular reactivity. Furthermore, histopathological abnormalities in the OLETF rats were prevented by KRG treatment. © 2019 The Korean Society of Ginseng, Published by Elsevier Korea LLC.Background Emerging evidence suggests that endothelial-to-mesenchymal transition (EndMT) in endothelial dysfunction due to persistent inflammation is a key component and emerging concept in the pathogenesis of vascular diseases. Ginsenoside Rg3 (Rg3), an active compound from red ginseng, has been known to be important for vascular homeostasis. However, the effect of Rg3 on inflammation-induced EndMT has never been reported. Here, we hypothesize that Rg3 might reverse the inflammation-induced EndMT and serve as a novel therapeutic strategy for vascular diseases. Methods EndMT was examined under an inflammatory condition mediated by the NOD1 agonist, γ-d-glutamyl-meso-diaminopimelic acid (iE-DAP), treatment in human umbilical vein endothelial cells. The expression of EndMT markers was determined by Western blot analysis, real-time polymerase chain reaction, and immunocytochemistry. The underlying mechanisms of Rg3-mediated EndMT regulation were investigated by modulating the microRNA expression. Results The NOD1 agonist, iE-DAP, led to a fibroblast-like morphology change with a decrease in the expression of endothelial markers and an increase in the expression of the mesenchymal marker, namely EndMT.